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Abstract

The amygdalae are an important component of the human limbic system and exhibit a key role in emotional and behavioral reactions. Previous studies have demonstrated abnormal function and morphology in the amygdalae of post‑traumatic stress disorder (PTSD)‑like animal models, however the underlying molecular mechanisms remain elusive. The authors have previously demonstrated that PTSD induced increased apoptosis in the amygdala of PTSD‑like animals. Cyclin D1 and cyclin‑dependent kinase 4 (CDK4) are two important regulators of the cell cycle. The study explored the expression of cyclin D1 and CDK4 in the amygdala in PTSD. The single‑prolonged stress (SPS) rat model was used as a PTSD‑like model. Ultrastructural alterations of cells in the amygdala were observed using transmission electron microscopy (TEM). 4',6‑Diamidino‑2‑phenylindole (DAPI) fluorescence was employed to detect nuclear pycnosis. Cyclin D1 and CDK4 expression in the amygdala cells was examined using immunofluorescence, Western blotting and reverse transcription‑quantitative polymerase chain reaction. TEM revealed morphological alterations to the amygdala cells of the SPS rats. DAPI‑stained nuclear brightness levels differed between the control and SPS groups. Expression of cyclin D1 and CDK4 in the amygdala increased gradually 1 day and 4 days following SPS stimulation, and peaked 7 days following SPS stimulation at the protein and mRNA levels, in comparison with the control rats. These findings suggest that SPS resulted in increased cyclin D1 and CDK4 expression, which may accelerate cell apoptosis. This may be associated with SPS‑induced abnormal function and structure of the amygdala.